• Users Online: 71
  • Print this page
  • Email this page


 
 
Table of Contents
EDITORIAL
Year : 2021  |  Volume : 7  |  Issue : 2  |  Page : 39-42

Adverse conditions and pregnancy and vice versa


Department of Nephrology, SGPGIMS, Lucknow, Uttar Pradesh, India

Date of Submission02-Feb-2022
Date of Acceptance02-Feb-2022
Date of Web Publication25-Feb-2022

Correspondence Address:
Prof. Anita Saxena
Department of Nephrology, SGPGIMS, Lucknow, Uttar Pradesh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jrnm.jrnm_2_22

Rights and Permissions

How to cite this article:
Saxena A. Adverse conditions and pregnancy and vice versa. J Renal Nutr Metab 2021;7:39-42

How to cite this URL:
Saxena A. Adverse conditions and pregnancy and vice versa. J Renal Nutr Metab [serial online] 2021 [cited 2022 May 26];7:39-42. Available from: http://www.jrnm.in/text.asp?2021/7/2/39/338551





Hippocrates stated “our natures are the real physician of our diseases.” Pregnancy is a hyperdynamic, hypervolemic state with a growing fetus as a new life and cascade of anatomic and physiological alterations. Hormonal influences and the obstructive effect of the enlarging uterus, cause an increase in kidney volume, weight, and marked dilation of ureters (affecting up to 90% of women) and renal calyces which ensue as early as the first trimester.[1],[2]

Renal adaptation during pregnancy and immediately postpartum is witnessed as increased kidney size by approximately 1 cm.[3]

During the advancing course of pregnancy, the enlarging uterus exerts compressive effect on the aortavena cava which decreases effective renal blood flow by 20%.[4]

However, the substantial increase in the glomerular filtration rate accompanies the increase in renal blood flow, changes in blood urea nitrogen (BUN), serum creatinine values, and lower uric acid levels. Creatinine clearance may decrease by approximately 20% with serum values of BUN and serum creatinine falling in the last few weeks of the third trimester.[5] Several physiological adaptations take place in the kidneys like tubular function and handling of water and electrolytes, alteration in acid-base, leading to mild increases in proteinuria, glucosuria, lower serum osmolality, and reductions in serum sodium levels. Decreased serum osmolality results in increased metabolism of placental vasopressinase (AVP) between the 4th and 38th weeks of gestation, which may result in transient diabetes insipidus featuring as polydipsia and polyuria with serum osmolality higher than 285 mOsm/L associated with hyposthenuria.[6] With residual urine retained within the collection system and the obstructive effect of the enlarging uterus predisposes the woman to urinary tract infections (UTI) and pyelonephritis.[3]

While physiological changes occurring in pregnancy influence normal biochemical values, the others may mimic symptoms of the medical disease such as serum creatinine >0.9 mg/dL and a BUN >14 mg/dL suggest preexisting renal disease or development of pregnancy-induced complications such as preeclampsia, warranting further evaluation to prevent adverse outcomes of pregnancy. The threshold of normal for protein excretion is twice that of the normal nonpregnant value (300 mg/24 h vs. 150 mg/24 h). The upper limit of normal for albumin excretion is 15% of nonpregnant values. It is, therefore, imperative to differentiate between normal physiological changes and disease pathology. The prevalence of asymptomatic bacteriuria during pregnancy is similar to that among nonpregnant women. Up to 3% of pregnancies are complicated by symptomatic UTI, including cystitis and pyelonephritis. AKI in pregnancy often presents with sepsis, volume contraction caused by hypovolemia and hemorrhage, urinary obstruction, pyelonephritis, preeclampsia/eclampsia, HELLP syndrome, and/or acute fatty liver of pregnancy. Only one case has been reported of minimal change disease (MCD) after abortion and another report of a patient with MCD without acute renal failure after elective termination of pregnancy has been documented.[7]

That women in childbirth were prone to fevers, the distinct name, “puerperal fever” appears in the times of Hippocrates who described puerperal sepsis as “Erysipelas attacking the internal surface of the pregnant uterus is destructive.”[8] Although the historical records appear only in the early eighteenth century.[9]

The medical treatises on puerperal fever which were published during the period from 1760 to 1850 and writings of Margaret DeLacy's[3] overview of puerperal fever in the eighteenth century appeared to cast light on the infectious nature of puerperal fever. The disease is currently believed to be caused by a bacterial infection of the upper genital tract, in which the most common causative organism is the beta hemolytic streptococcus, Lancefield Group A.[10],[11],[12],[13]

William Campbell, a physician from Edinburgh, in his treatise of 1822, recognized, to quote, that the symptoms of puerperal fever could be complex and difficult to interpret. In majority of patients the disease appeared on the 3rd day, and commenced with rigor, headache and the “cold fit” followed by extreme heat, perspiration, and thirst. Abdominal pain was an almost ubiquitous feature and this began as a mild symptom, becoming increasingly severe for the disease. This pain-which was accompanied by abdominal distension–was usually located in the hypogastric and iliac regions, and any apparent remission tended to be dangerous, indicating mortification.” There was “great derangement of the vascular system,” the pulse rising to as much as 140 beats per minute, and the patient tended to lie on her back and appear listless and indifferent. The tongue was usually white, although it could become dark and furred in the face of impending death. Respiration was difficult due to the abdominal pain and distension, and the patient was prone to nausea and vomiting. The early stages of the disease could be characterized by constipation, which, however, soon gave way to diarrhea. Urination was usually painful and the urine was “high colored and turbid.” The production of milk was usually suppressed, but the flow of lochia tended to continue. A minority of sufferers experienced delirium and mania.[14],[15],[16],[17],[18]

The well-known triad of fever, hemorrhage, and toxemia predominated in the past and is still to be found in some third world countries today.[11],[12],[13],[14],[15],[16] Between 35% and 55% of maternal deaths were due to puerperal sepsis (by far the most common cause of death), about 20% were due to toxemia, 20% to hemorrhage (ante-and postpartum) and the remainder to a variable group of other causes of which the most prominent was often abortion.[14]

Robert Ferguson opined that “any sort of damage or injury to the placenta during childbirth could have dangerous consequences, by setting up a reaction that led to puerperal fever, and that dangerous fluids of damaged, torn and subsequently inflamed arteries then circulate through the system. The diseased secretions from the traumatic surface irritate its large pendulous lacerated vessels, and give rise to the phenomena of puerperal fever.”[18],[20]

To elucidate the nature of fever and its management, inflammatory theory, stressing on the consistency of the blood and its action upon the arteries, appeared most plausible in the eighteenth century.

Stagnation and thickening of the blood of blood in any part of the system would cause increased pressure in the walls of the arteries in an attempt to re-establish proper circulation, which, if not swiftly resolved, would be transmitted throughout the circulation causing generalized pressure, accompanied by heat and if left unattended, the pressure would lead to a breakdown of the whole system. Major contributions to this concept were made by German physician and academic, Baron G F van Swieten. Later, the issue of whether puerperal fever was inflammatory or putrid resolved with the explanation that, if it was inflammatory, the fever was a pathological condition of the blood and circulation, that might have originated in the trauma of labor or damage to the uterus or other internal organs, but if it was putrid, the fever was caused by acrid or morbific matter in the system, or might simply be the result of the suppression of fluids or of obstructed perspiration,[21] and could also be part of a process of decay, or a body's attempt to throw off dangerous or poisonous matter.[22] Leake in his treatise elaborated on the origin of puerperal fever in inflammation as being related to stagnation of the blood, brought on by the “cold fit” of the fever. He further explained that “puerperal fever began as inflammation of the abdominal viscera, more particularly, of the omentum, which was caused by the plethora of the blood and that inflammation resulted in suppuration which could increase in putrescency and then become infectious.[23]” Texts by Boerhaave state Inflammation as “phlegmon” or “fire” and consisted of greater pressure and attrition of the red arterial blood, stagnating in the smallest vessels, and urged by the motion of the rest of the blood,” and to Swieten, if inflammation affected internal viscera, fever almost invariably ensued. Terminations” of inflammation, could take any of three forms, resolution, suppuration or “gangrene.”[24],[25]

Herman Boerhaave compared the human body with a machine, depicting the circulatory system as a part that behaved like a set of fluid hydraulic devices, and disease as a disorder in the functioning of this system. Mechanical stress featuring pregnancy and delivery as pressure of the fetus on the abdominal and pelvic viscera and the damage to tissue caused by delivery is documented in the doctrines of Herman Boerhaave, as the causes of inflammation. “Along with the local inflammation of the abdominal viscera, the diversion of a large volume of blood into the lower abdomen caused deficiency particularly in the heart and brain, which was rapidly followed by an over-compensation and the pooling of blood in these organs once more, accompanied by “anxiety and oppression at the breast and praecordia.”[23] The “cold fit” which followed was caused by the draining of blood from the extremities. Vomiting and diarrhea result from pooling of blood in the “vena portae ventralis,” leading to the excessive secretion of bile. That inflammatory process of puerperal fever began as a mechanistic and hydraulic movements of blood within the circulatory system, suggestive of an almost tidal sense of blood washing rapidly into and out of the small vessels, creating alternately heat and cold, pain and relaxation. In this way, the physician makes sense of the apparently confusing symptoms of fever with its hot and cold fits and its localized pains and generalized discomfort is seen in Leake's description of the effects of puerperal fever offers a vivid account of mechanistic.[23],[26]

Writings of Hulme and Leake and Denman state that “puerperal fever begins as an inflammatory condition, but progresses to a putrid disease after some days.”[27] Robert Gooch in the 19th century opined that puerperal fever was a disorder of the peritoneum and therefore it should more accurately be named “peritoneal fever.”

Both ancient and modern writers tended to divide fevers into “putrid” and “nonputrid” fevers, but where was any mention on norms for feeding a growing fetus in a renal compromised woman? Hippocrates (460-370 B. C.) believed that fetus “sucks nutrition from “uterine paps” (“Pneuma”) or the cotyledons of the decidua[28] formed by subepithelial cells of the uterine lining during pregnancy. Aristotle (384-322 BC) was the first to postulate the delivery of nutrition through the umbilical cord. The Renaissance marked the beginning of rapid progress in understanding the structure and function of the placenta,[14],[29] Pregnancy involves caring for two evolving lives therefore, dietary protein intake should not be restricted during pregnancy in women with diabetes and chronic kidney disease (CKD). There are no studies on pregnant diabetics CKD Stage 5. Strategies for the management of hyperglycemia, hypertension, and dyslipidemia are extrapolated from the recommendations for women with earlier stages of CKD. Limitation of dietary protein in women with diabetes and CKD should be liberalized during pregnancy to ensure adequate nutrition for the fetus. In the opinion of the KDOQI Work Group, these patients should be counseled to increase their intake of protein to 1–1.2 g/kg (prepregnancy weight) per day and energy intake, and other nutrients like iron, calcium, and water-soluble vitamins as for non-CKD pregnant woman.[30] If the patient has AKI hyperkalemia, hyperphosphatemia, and metabolic acidosis can be present. Hyperkalemia in the presence of ECG changes requires pharmacological intervention with 10% calcium gluconate to stabilize the cardiac membrane. The standard urgent intervention for potassium levels of 6 mEq/L or greater is sodium bicarbonate, intravenous glucose, and insulin along with dietary restriction (restrict potassium-rich fruits and vegetables) to prevent its recurrence. Hyperkalemia may also necessitate dialysis. The use of phosphate binders if the patient is stable (in the absence of nausea and vomiting) is the usual conservative medical approach for hyperphosphatemia. Correction of metabolic acidosis may require bicarbonate therapy or dialysis if volume overload or pulmonary edema are unresponsive to traditional diuretic therapy, or if uremia is present.[31],[32]

Pharmacological treatment of lipid abnormalities during pregnancy is not currently recommended due to potential risks to the fetus.[33],[34] Nevertheless, maternal hypercholesterolemia is associated with the development of fetal atherosclerosis[33],[34] so this recommendation may change as results of additional studies of statins and other agents during pregnancy become available. However, until such studies are available, the Work Group opines that statins and other lipid-lowering therapies should be discontinued after a missed menstrual period or a positive pregnancy test result in women with diabetes and CKD. Women and adolescent girls with childbearing potential who are treated with lipid-lowering therapies should be counseled about these risks.

This issue brings to you a short review on “approach to pregnancy in patient with CKD” which briefly describes the effect of CKD on pregnancy and approach for a successful pregnancy. This issue also carries a short review on the pathophysiology of renovascular hypertension and a tutorial on the effect of uremic toxins on nutritional status and an article on the integrative approach to detect protein-energy wasting among CKD maintenance hemodialysis patients.



 
  References Top

1.
Faúndes A, Brícola-Filho M, Pinto e Silva JL. Dilatation of the urinary tract during pregnancy: Proposal of a curve of maximal caliceal diameter by gestational age. Am J Obstet Gynecol 1998;178:1082-6.  Back to cited text no. 1
    
2.
Conklin K. Physiologic changes of pregnancy. In: Chestnut D, editors. Obstetric Anesthesia: Principles and Practice. St. Louis: Mosby; 1994. p. 17-42.  Back to cited text no. 2
    
3.
Lindheimer M, Grunfeld J, Davison J. Renal disorders. In: Barron W, Lin M, Davison J, editors. Medical Disorders during Pregnancy. 3rd ed. St. Louis: Mosby; 2000. p. 39-70.  Back to cited text no. 3
    
4.
Chesley L. Renal functional changes in normal pregnancy. Clin Obstet Gynecol 1960;3:349.  Back to cited text no. 4
    
5.
Kincaid-Smith P, Fairley K. The Kidney and Hypertension in Pregnancy. Edinburgh, Scotland: Churchill Livingstone; 1993.  Back to cited text no. 5
    
6.
Ananthakrishnan S. Diabetes insipidus during pregnancy. Best Pract Res Clin Endocrinol Metab 2016;30:305-15.  Back to cited text no. 6
    
7.
Greenberg S, Jana KR, Janga KC, Kumar K. Minimal change disease after elective surgical abortion: A case report. Am J Case Rep 2021;22:e930292.  Back to cited text no. 7
    
8.
Dunn PM. Hippocrates (460-c 356 BC) and the founding of perinatal medicine. Arch Dis Child 1993;69:540-1.  Back to cited text no. 8
    
9.
Irvine Loudon. The debate about when the term Childbed Fever was first used In: The Tragedy of Childbed Fever. Oxford University Press; 2000. p. 8.  Back to cited text no. 9
    
10.
Lansing DI, Penman WR, Davis DJ. Puerperal fever and the Group B beta hemolytic streptococcus. Bull Hist Med 1983;57:70-80.   Back to cited text no. 10
    
11.
DeLacy M. Puerperal fever in eighteenth-century Britain. Bull Hist Med 1989;63:521-56.  Back to cited text no. 11
    
12.
Lowis GW. Epidemiology of puerperal fever: The contributions of Alexander Gordon. Med Hist 1993;37:399-410.  Back to cited text no. 12
    
13.
Seligman SA. The lesser pestilence: Non-epidemic puerperal fever. Med Hist 1991;35:89-102.  Back to cited text no. 13
    
14.
Loudon I. On maternal and infant mortality, 1900-1960. Soc Hist Med 1991;4:29-73.  Back to cited text no. 14
    
15.
Loudon I. Deaths in childbed from the eighteenth century to 1935. Med Hist 1986;30:1-41.  Back to cited text no. 15
    
16.
Loudon I. Puerperal fever, the streptococcus, and the sulphonamides, 1911-1945. Br Med J (Clin Res Ed) 1987;295:485-90.  Back to cited text no. 16
    
17.
Loudon I. Maternal mortality: 1880-1950. Some regional and international comparisons. Soc Hist Med 1988;1:183-228.  Back to cited text no. 17
    
18.
Hallett C. The attempt to understand puerperal fever in the eighteenth and early nineteenth centuries: The influence of inflammation theory. Med Hist 2005;49:1-28.  Back to cited text no. 18
    
19.
Lee R. Clinical reports of difficult cases in midwifery. Lond Med Gaz 1838-39;2:554-908-10.  Back to cited text no. 19
    
20.
Joseph Clarke. Observations on the puerperal fever', Edinburgh Medical Commentaries, 1790, 15: 299, reprinted in Churchill (ed.), pp. 351–62, esp. pp. 355–6.  Back to cited text no. 20
    
21.
Fordyce W. In: Cadell T, Murray J, Davenhill W, editors. A New Inquiry into the Causes, Symptoms, and Cure of Putrid and Inflammatory Fevers. 4th ed. London:1777. p. 48-53.  Back to cited text no. 21
    
22.
Kirkland T. An Essay towards an Improvement in the Cure of those Diseases which are the Cause of Fevers. London: Dodesley J; 1767. p. 31.  Back to cited text no. 22
    
23.
Jhon L. In: Churchill, editor. Observations on the Child-Bed Fever. 1772. p. 145.  Back to cited text no. 23
    
24.
Hunt J. Boerhaave, academical lectures. In: Johnson J, Elliot C, editors. Observations on the Circulation of the Blood. London, Edinburgh: 1787.  Back to cited text no. 24
    
25.
Cullen W. In: Elliot C, editor. Institutions of Medicine. Part I: Physiology. 3rd ed. Edinburgh, London: Cadell T; 1785. p. 192-4.  Back to cited text no. 25
    
26.
Oliver W Holmes, 'The contagiousness of puerperal fever', Medical Classics, 1937–37, 1: 211–43, reprinted from the N. England Q. J Med. Surg., 1843, 1 (4): 503–30; idem, 'Puerperal fever as a private pestilence', Medical Classics, 1936–37, 1: 211–68.  Back to cited text no. 26
    
27.
Denman T. Essays on the Puerperal Fever and Puerperal Convulsions. London: Walter J; 1768. p. 8-10.  Back to cited text no. 27
    
28.
de Witt F. An historical study on theories of the placenta to 1900. J Hist Med Allied Sci 1959;14:360-74.  Back to cited text no. 28
    
29.
Mir IN, Chalak L. Placenta-'The least understood human organ'-from animistic origins to human placental project. Ann Reprod Med Treat 2017;2:1013.  Back to cited text no. 29
    
30.
Nelson RG, Tuttle KR, Aschner P, Bakris GL, Bilous R, Caramori ML. KDOQI clinical practice guidelines and clinical practice recommendations for diabetes and chronic kidney disease. Am J Kidney Dis 2007;49 Suppl 2:S12-154.  Back to cited text no. 30
    
31.
Thorsen MS, Poole JH. Renal disease in pregnancy. J Perinat Neonatal Nurs 2002;15:13-26.  Back to cited text no. 31
    
32.
Napoli C, D'Armiento FP, Mancini FP, Postiglione A, Witztum JL, Palumbo G, et al. Fatty streak formation occurs in human fetal aortas and is greatly enhanced by maternal hypercholesterolemia. Intimal accumulation of low density lipoprotein and its oxidation precede monocyte recruitment into early atherosclerotic lesions. J Clin Invest 1997;100:2680-90.  Back to cited text no. 32
    
33.
Levitt NS, Bradshaw D, Zwarenstein MF, Bawa AA, Maphumolo S. Audit of public sector primary diabetes care in Cape Town, South Africa: high prevalence of complications, uncontrolled hyperglycaemia, and hypertension. Diabet Med 1997;14:1073-7.  Back to cited text no. 33
    
34.
Clark S, Cotton D, Hankins G, Phelan J. Acute renal failure. In: Clark S, Cotton D, Hankins G, Phelan J, editors. Critical Care Obstetrics. 3rd ed. Malden, MA: Blackwell Science; 1997. p. 314-24.  Back to cited text no. 34
    




 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
References

 Article Access Statistics
    Viewed383    
    Printed26    
    Emailed0    
    PDF Downloaded43    
    Comments [Add]    

Recommend this journal